LncRNA SENCR suppresses abdominal aortic aneurysm formation by inhibiting smooth muscle cells apoptosis and extracellular matrix degradation

• Main Authors: Zhou Cai, Jianhua Huang, Junxiao Yang, Baihong Pan, Wei Wang, Yangyang Ou, Xianwei Wang, Pu Yang
• Format: Article
• Language: English
• Published: Association of Basic Medical Sciences of Federation of Bosnia and Herzegovina 2020-09-01
• Series: Bosnian Journal of Basic Medical Sciences
• Subjects: Abdominal aortic aneurysm; lncRNA SENCR; vascular smooth muscle cells; cell apoptosis; extracellular matrix degradation
• Online Access: https://www.bjbms.org/ojs/index.php/bjbms/article/view/4994

Abdominal aortic aneurysm (AAA) is a progressive chronic dilatation of the abdominal aorta without effective medical treatment. This study aims to clarify the potential of long non-coding RNA SENCR as a treatment target in AAA. Angiotensin II (Ang-II) was used to establish AAA mouse model as well as a cell model based on the mouse aortic vascular smooth muscle cells (VSMCs). Reverse transcription quantitative PCR and western blot were performed to measure the expression of SENCR and proteins, respectively. Apoptotic rate in VSMCs was determined using Annexin V-FITC/PI double staining, and cell apoptosis in aortic tissues was determined by TUNEL staining. Hematoxylin and eosin and Elastica van Gieson staining were used for histological analysis of aortic tissues. SENCR was downregulated in AAA tissues and Ang-II-stimulated VSMCs. Overexpression of SENCR inhibited Ang-II-induced VSMC apoptosis, while inhibition of SENCR facilitated VSMC apoptosis. Moreover, overexpression of SENCR suppressed matrix metalloproteinase (MMP)-2 and MMP-9 expression and promoted tissue inhibitor of metalloproteinases 1 (TIMP-1) expression in Ang-II-induced VSMCs, while inhibition of SENCR expression led to the opposite results. In vivo, overexpressed SENCR improved the pathological change in aortic tissues and the damage in arterial wall elastic fibres induced by Ang-II, as well as it suppressed Ang-II-induced cell apoptosis and extracellular matrix degradation in aortic tissues. Overall, overexpression of SENCR inhibited AAA formation via suppressing VSMC apoptosis and extracellular matrix degradation. We provided a reliable evidence for SENCR acting as a potential target for AAA treatment.